Prediction of oxygen supplementation by a deep-learning model integrating clinical parameters and chest CT images in COVID-19.

PURPOSE: As of March 2023, the number of patients with COVID-19 worldwide is declining, but the early diagnosis of patients requiring inpatient treatment and the appropriate allocation of limited healthcare resources remain unresolved issues. In this study we constructed a deep-learning (DL) model to predict the need for oxygen supplementation using clinical information and chest CT images of patients with COVID-19. MATERIALS AND METHODS: We retrospectively enrolled 738 patients with COVID-19 for whom clinical information (patient background, clinical symptoms, and blood test findings) was available and chest CT imaging was performed. The initial data set was divided into 591 training and 147 evaluation data. We developed a DL model that predicted oxygen supplementation by integrating clinical information and CT images. The model was validated at two other facilities (n = 191 and n = 230). In addition, the importance of clinical information for prediction was assessed. RESULTS: The proposed DL model showed an area under the curve (AUC) of 89.9% for predicting oxygen supplementation. Validation from the two other facilities showed an AUC > 80%. With respect to interpretation of the model, the contribution of dyspnea and the lactate dehydrogenase level was higher in the model. CONCLUSIONS: The DL model integrating clinical information and chest CT images had high predictive accuracy. DL-based prediction of disease severity might be helpful in the clinical management of patients with COVID-19.

Thoracic empyema caused by Alloscardovia omnicolens and Bifidobacteriumdentium.

A 62-year-old man was admitted to our emergency department with the complaint of worsening dyspnea after initiating anti-tuberculous therapy (isoniazid [300 mg/day], rifampicin [600 mg/day], ethambutol [750 mg/day], and pyrazinamide [1,500 mg/day]) for tuberculous pleuritis. His oral hygiene status was poor. The patient had no significant past medical history. However, he had a history of smoking (10 cigarettes per day for 45 years) and was a social drinker. Chest radiography revealed increased right pleural effusion and pneumothorax. The pleural fluid was purulent, and the culture grew Alloscardovia omnicolens, Bifidobacterium dentium, and Prevotella loescheii. He was treated with antibiotics (3 g of intravenous ampicillin/sulbactam every 6 h, which was changed to oral amoxicillin/clavulanate potassium on day 34) in addition to anti-tuberculous therapy, he underwent chest tube insertion, and subsequently improved. Bifidobacteriaceae are commensal flora of the mouth and pulmonary infections caused by these organisms are extremely rare. Nevertheless, clinicians should consider these organisms as a possible cause of pulmonary infections, and consider that respiratory infections caused by commensal flora of the mouth may occur during the treatment of other diseases in patients with poor oral hygiene.

Advanced stage of chronic kidney disease is risk of poor treatment outcome for smear-positive pulmonary tuberculosis.

Chronic kidney disease (CKD) is an increased risk for the development of active tuberculosis, but few studies have analyzed the treatment outcome of pulmonary tuberculosis among CKD patients. A retrospective cohort study was conducted at Chiba-East Hospital in Chiba, Japan. Our study estimated the treatment outcomes in smear-positive pulmonary tuberculosis in relation to CKD and its stages. Total subjects were 759 patients (12-99 years) hospitalized between 2007 and 2012. Patients suffering from multi-drug-resistant tuberculosis were excluded. Patients with CKD were 19.3% aged <65 years (n = 384), and 49.6% aged ≥ 65 years, respectively (P < 0.001). Successful treatment was 52.7% in CKD (n = 260) and 67.3% in non-CKD (n = 499) (P < 0.001). Death was 25.4% in CKD and 12.4% in non-CKD (P < 0.001). Treatment outcome was especially poor in patients with low estimated glomerular filtration rate (eGFR) of <30 ml/min/1.73 m(2), as successful treatment was 20.0%, and death was 50.0%, significantly lower than in other CKD and non-CKD patients. After multivariate logistic regression analysis, eGFR<30 ml/min/1.73 m(2) was an independent factor affecting successful treatment and death, and its adjusted odds ratios (aOR) were 0.20 (95% confidence interval (CI) 0.07-0.50) and 2.99 (95%CI 1.20-7.51), respectively. Other factors affecting successful treatment were serum albumin <3.0 mg/dl, steroid therapy for underlying disease and cardiovascular disease, with aOR (95%CI) of 0.28 (0.20-0.39), 0.32 (0.16-0.63) and 0.49 (0.28-0.86), respectively. Several factors were associated with poor treatment outcome of smear-positive pulmonary tuberculosis. Advanced stage of CKD with eGFR of <30 ml/min/1.73 m(2) was a risk factor for poor treatment outcome.

Inhalation of Stachybotrys chartarum evokes pulmonary arterial remodeling in mice, attenuated by Rho-kinase inhibitor.

Stachybotrys chartarum, a ubiquitous fungus in our environment, has been suspected of causing respiratory symptoms in humans, such as acute infant pulmonary hemorrhage and asthma. We previously established a mouse model in which repeated inhalation of Stachybotrys chartarum spores caused pulmonary hypertension. To further investigate the model, particularly in the pulmonary circulation, mice were intra-tracheally injected with spores, 18 times over 12 weeks. Severe muscularization was observed in the small- to medium-sized pulmonary arteries. Bronchoalveolar lavage fluid revealed an increase in eosinophils accompanied by high concentrations of Th2-associated cytokines, IL-4, IL-5, but not Th1-associated IFN-γ. The remodeling was temporary, resolving after cessation of spore inhalation. Chronic inhibition of the RhoA/Rho-kinase pathway by fasudil attenuated pulmonary arterial remodeling. These data suggest that Stachybotrys-mediated remodeling is caused by Th2-associated inflammation and can be resolved by Rho-kinase inhibition, either through direct effects on smooth muscle hypertrophy or through indirect effects on vascular inflammation. These data also show that extensive pulmonary vascular remodeling, often thought of as a fixed lesion, will spontaneously resolve in the absence of underlying molecular etiology.

[Candidates for virulence factors of Aspergillus fumigatus].

The number of patients with invasive fungal infection (IFI) has dramatically increased since the beginning of the 1980s. Aspergillus fumigatus, the most common species recovered from aspergillosis, is an important pathogen of IFI. Recently, new antifungal agents have become available in Japan, but mortality from aspergillosis is still high. Early initiation of therapy seems to improve the survival rate. Study of virulence factors of the fungus may lead to the development of novel diagnostic tools or advancements in therapy. Many candidates of the fungal virulence factors have been studied including proteases and mycotoxins. We previously discussed the influence of fungal secondary metabolites such as gliotoxin and other low molecular components on the virulence, and showed that A. fumigatus produces potent cytotoxic substances other than gliotoxin. Studies are in progress to clarify the significance of the unknown substances.

Inhalation of Stachybotrys chartarum causes pulmonary arterial hypertension in mice.

Inhalation of Stachybotrys chartarum, a ubiquitous fungus in our living environment, has been suspected as a cause of acute idiopathic pulmonary haemorrhage in infants, but its relation to human diseases is not yet known. The aim of present study was to investigate the effect of repeated intratracheal injection of the fungus into mice, paying special attention to the pulmonary vascular system. Spores of S. chartarum were injected into the trachea of mice from 6 to 18 times over 4-12 weeks, and the lungs were examined by histopathology, morphometrics and haemodynamics. When 1 x 10(4) spores/mouse were injected, histopathological examination showed the development of pulmonary arterial hypertension (PAH). Symmetrical thickening of the intima and media of the pulmonary arterial walls was seen after six injections over 4 weeks. Right ventricular hypertrophy was also evident after 12 injections. PAH was confirmed by the elevation of right ventricular systolic pressure (20.1 +/- 5.7 mmHg in the injected group vs. 12.0 +/- 2.4 mmHg in the control group, P < 0.01). This study showed that the inhalation of S. chartarum caused PAH in mice, suggesting a potential of S. chartarum as a cause of human health problem such as PAH.

Macroscopic and histological findings in the healing process of inhalation injury.

Although many investigators reported the diagnostic and therapeutic value of bronchoscopy in the early stage of inhalation injury, few findings in the late stage of inhalation injury have been reported. We investigated histopathological changes of in trachea and bronchi after inhalation injury. Five survivors with inhalation injury underwent bronchoscopic examinations combined with biopsies from the early stage to the late stage. Although the bronchotracheal membranes improved to near normal under the bronchoscopic findings in the late or recovery stage, invasion of inflammatory cells and the capillary dilatation in the subepithelial region were still remarkable histologically. Goblet cells also increased on the surface of mucous membranes. In cases of the inhalation injury with severe burn, pulmonary edema, bronchial edema and secretions tended to be prolonged. Results suggested that continuous secretions in the respiratory tracts sometimes cause airway obstruction. Bronchoscopic and histologic findings in the healing process of inhalation injury predict long-term pulmonary functional outcome. Moreover, the aggressive pulmonary toilet seemed to be effective in removing foreign particles and accumulated secretions which also cause the inflammatory response and the obstruction in inhalation injury.